Epilepsy is characterized by a tendency to recurrent seizures that can lead to loss of awareness, loss of consciousness, and/or disturbances of movement, autonomic function, sensation (including vision, hearing and taste), mood, and/or mental function. Epilepsy afflicts 1–2% of the population in the developed world. The mean prevalence of active epilepsy (i.e., continuing seizures or the need for treatment) in developed and undeveloped countries combined is estimated to be 7 per 1,000 of the general population, or approximately 40 million people worldwide. Studies in developed countries suggest an annual incidence of epilepsy of approximately 50 per 100,000 of the general population. However, studies in developing countries suggest this figure is nearly double at 100 per 100,000.
The primary pathology of epilepsy is a synchronization of electrical activity between large numbers of brain neurons. Neurons “fire”, i.e., transmit an electrical depolarization pulse down an axon(s), multiple times per second. While a group of adjacent neurons may normally demonstrate some correlation in their firing pattern, they normally do not all fire with exactly the same rate and exactly the same timing. However, during a seizure, a group of neurons in the brain demonstrate a highly synchronized firing pattern. This group may be localized, in which case it may be referred to as the seizure focus. In some types of epilepsy, the focus may remain fixed. In other types of epilepsy, the patient may have multiple fixed foci, and a seizure may arise from any of the foci. In still other types of epilepsy, a seizure may arise from a seemingly random location. Finally, in some types of epilepsy the seizure appears to arise from a majority of the brain all at once, i.e., with no focus. Seizures that arise from a focus may remain localized, in which case the symptoms of the seizure depend on the site of the focus. Seizures that arise from a focus may also spread to the majority of the brain, i.e., it may be initially focal but become secondarily generalized.
Epilepsy is often but not always the result of underlying brain disease. Any type of brain disease can cause epilepsy, but not all patients with the same brain pathology will develop epilepsy. The cause of epilepsy cannot be determined in a number of patients; however, the most commonly accepted theory posits that it is the result of an imbalance of certain chemicals in the brain, e.g., neurotransmitters. Children and adolescents are more likely to have epilepsy of unknown or genetic origin. The older the patient, the more likely it is that the cause is an underlying brain disease such as a brain tumor or cerebrovascular disease.
Trauma and brain infection can cause epilepsy at any age, and in particular, account for the higher incidence rate in developing countries. For example, in Latin America, neurocysticercosis (cysts on the brain caused by tapeworm infection) is a common cause of epilepsy; in Africa, AIDS and its related infections, malaria and meningitis, are common causes; in India, AIDS, neurocysticercosis, and tuberculosis are common causes. Febrile illness of any kind, whether or not it involves the brain, can trigger seizures in vulnerable young children, which seizures are called febrile convulsions. About 5% of such children go on to develop epilepsy later in life. Furthermore, for any brain disease, only a proportion of sufferers will experience seizures as a symptom of that disease. It is therefore suspected that those who do experience such symptomatic seizures are more vulnerable for similar biochemical/neurotransmitter reasons.
A number of U.S. patents have addressed using electrical and/or drug stimulation to increase and/or decrease excitement of various brain structures to treat epilepsy. For instance, U.S. Pat. Nos. 5,713,923 and 5,978,702 teach decreasing excitement/activity (or increasing inhibition) of the seizure focus, the globus pallidus interna (GPi), the substantia nigra reticulata (SNr), the anterior thalamic nucleus, the subthalamic nucleus (STN), and the neostriatum and increasing excitement/activity (or decreasing inhibition) of the ventrolateral (VL) thalamus, stiatopallidal fiber pathway, neostratium, the globus pallidus externa (GPe), and the GPe to STN fiber pathway. U.S. Pat. Nos. 5,800,474 and 5,752,979 teach blocking STN activity to reduce excitement of the SNr; the later does this by increasing GPe activity.
While these various treatment locations, methods, and systems exist, the inventors believe that enhanced systems, alternative locations, and modified methods will lead to improved treatment of epilepsy.